Vitamin B12 is the cofactor in enzymatic reactions with diverse physiological functions. It is required for the conversion of methylmalonyl CoA to succinyl CoA, as well as for the conversion of homocysteine to methionine by methionine synthase, which is then converted into S-adenosylmethionine. A B12 deficiency causes impairments in both of these pathways, disrupting neurological function, including poor formation of myelin nerve sheaths, production of toxic levels of homocysteine, and inefficient energy production in all cells. Methylcobalamin, the principal circulating form of B12 and the one transported into peripheral tissues, has been shown to not only reduce homocysteine, but also to reduce inflammatory factors and the volume of carotid artery plaques among stroke patients, as well as pain, and neuropathy among diabetics.

Cobalamin is also required to remove the methyl group from methyltetrahydrofolate and generate tetrahydrofolate, a necessary step in DNA synthesis. As a consequence, B12 deficiency affects the growth, function, and repair of all cells, the most apparent sign of which is megaloblastic anemia, caused by inhibited mitosis of red blood cells.9 Some individuals, especially those with malabsorption or low dietary intake, are at higher risks for a B12 deficiency. B12 in sublingual form, at a dose of 1000 mcg per day bypasses active absorption routes, and can restore normal B12 levels even in those with gastric bypass, pernicious anemia and/or impaired absorptive capacity, with greater effectiveness than even intramuscular injection